Actaea racemosa L. extract inhibits steroid sulfation in human breast cancer cells: Effects on androgen formation.


Journal

Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794

Informations de publication

Date de publication:
Dec 2020
Historique:
received: 29 03 2020
revised: 26 08 2020
accepted: 24 09 2020
pubmed: 5 10 2020
medline: 17 12 2020
entrez: 4 10 2020
Statut: ppublish

Résumé

Actaea racemosa L., also known as black cohosh, is a popular herb commonly used for the treatment of menopausal symptoms. Because of its purported estrogenic activity, black cohosh root extract (BCE) may trigger breast cancer growth. The potential effects of standardized BCE and its main constituent actein on cellular growth rates and steroid hormone metabolism were investigated in estrogen receptor alpha positive (ERα+) MCF-7 and -negative (ERα-) MDA-MB-231 human breast cancer cells. Cell numbers were determined following incubation of both cell lines with the steroid hormone precursors dehydroepiandrosterone (DHEA) and estrone (E1) for 48 h, in the presence and absence of BCE or actein. Using a validated liquid chromatography-high resolution mass spectrometry assay, cell culture supernatants were simultaneously analyzed for the ten main steroids of the estrogen pathway. Inhibition of MCF-7 and MDA-MB-231 cell growth (up to 36.9%) was observed following treatment with BCE (1-25 µg/ml) or actein (1-50 µM). Incubation of MCF-7, but not of MDA-MB-231 cells, with DHEA and BCE caused a 20.9% reduction in DHEA-3-O-sulfate (DHEA-S) formation, leading to a concomitant increase in the androgens 4-androstene-3,17-dione (AD) and testosterone (T). Actein was shown to exert an even stronger inhibitory effect on DHEA-S formation in MCF-7 cells (up to 89.6%) and consequently resulted in 12- to 15-fold higher androgen levels compared with BCE. The formation of 17β-estradiol (E2) and its glucuronidated and sulfated metabolites was not affected by BCE or actein after incubation with the estrogen precursor estrone (E1) in either cell line. The results of the present study demonstrated that actein and BCE do not promote breast cancer cell growth or influence estrogen levels. However, androgen formation was strongly stimulated by BCE and actein, which may contribute to their ameliorating effects on menopausal symptoms in women. Future studies monitoring the levels of AD and T upon BCE supplementation of patients are warranted to verify an association between BCE and endogenous androgen metabolism.

Sections du résumé

BACKGROUND BACKGROUND
Actaea racemosa L., also known as black cohosh, is a popular herb commonly used for the treatment of menopausal symptoms. Because of its purported estrogenic activity, black cohosh root extract (BCE) may trigger breast cancer growth.
STUDY DESIGN/METHODS METHODS
The potential effects of standardized BCE and its main constituent actein on cellular growth rates and steroid hormone metabolism were investigated in estrogen receptor alpha positive (ERα+) MCF-7 and -negative (ERα-) MDA-MB-231 human breast cancer cells. Cell numbers were determined following incubation of both cell lines with the steroid hormone precursors dehydroepiandrosterone (DHEA) and estrone (E1) for 48 h, in the presence and absence of BCE or actein. Using a validated liquid chromatography-high resolution mass spectrometry assay, cell culture supernatants were simultaneously analyzed for the ten main steroids of the estrogen pathway.
RESULTS RESULTS
Inhibition of MCF-7 and MDA-MB-231 cell growth (up to 36.9%) was observed following treatment with BCE (1-25 µg/ml) or actein (1-50 µM). Incubation of MCF-7, but not of MDA-MB-231 cells, with DHEA and BCE caused a 20.9% reduction in DHEA-3-O-sulfate (DHEA-S) formation, leading to a concomitant increase in the androgens 4-androstene-3,17-dione (AD) and testosterone (T). Actein was shown to exert an even stronger inhibitory effect on DHEA-S formation in MCF-7 cells (up to 89.6%) and consequently resulted in 12- to 15-fold higher androgen levels compared with BCE. The formation of 17β-estradiol (E2) and its glucuronidated and sulfated metabolites was not affected by BCE or actein after incubation with the estrogen precursor estrone (E1) in either cell line.
CONCLUSIONS CONCLUSIONS
The results of the present study demonstrated that actein and BCE do not promote breast cancer cell growth or influence estrogen levels. However, androgen formation was strongly stimulated by BCE and actein, which may contribute to their ameliorating effects on menopausal symptoms in women. Future studies monitoring the levels of AD and T upon BCE supplementation of patients are warranted to verify an association between BCE and endogenous androgen metabolism.

Identifiants

pubmed: 33011631
pii: S0944-7113(20)30188-4
doi: 10.1016/j.phymed.2020.153357
pii:
doi:

Substances chimiques

Androgens 0
Antineoplastic Agents, Phytogenic 0
ESR1 protein, human 0
Estrogen Receptor alpha 0
Plant Extracts 0
Saponins 0
Steroids 0
Triterpenes 0
Estradiol 4TI98Z838E
Sulfotransferases EC 2.8.2.-
alcohol sulfotransferase EC 2.8.2.2
actein I14QO4LW9V

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

153357

Subventions

Organisme : Austrian Science Fund FWF
ID : I 3417
Pays : Austria

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier GmbH.. All rights reserved.

Auteurs

Stefan Poschner (S)

Department of Pharmaceutical Chemistry, University of Vienna, 1090 Vienna, Austria.

Judith Wackerlig (J)

Department of Pharmaceutical Chemistry, University of Vienna, 1090 Vienna, Austria.

Daniel Dobusch (D)

Department of Pharmaceutical Chemistry, University of Vienna, 1090 Vienna, Austria.

Bettina Pachmann (B)

Department of Pharmaceutical Chemistry, University of Vienna, 1090 Vienna, Austria.

Santosa J Banh (SJ)

Department of Pharmaceutical Chemistry, University of Vienna, 1090 Vienna, Austria.

Theresia Thalhammer (T)

Department of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, 1090 Vienna, Austria.

Walter Jäger (W)

Department of Pharmaceutical Chemistry, University of Vienna, 1090 Vienna, Austria; Vienna Metabolomics Center (VIME), University of Vienna, 1090 Vienna, Austria. Electronic address: walter.jaeger@univie.ac.at.

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Classifications MeSH